Many interactions between plants and microbes begin with specific recognition. The nature of this recognition, and the interpretation of subsequent signal transduction by both plant and microbe have profound impact on the outcome of the interaction. Plants have evolved effective mechanisms to recognize pathogenic microbes and halt their biotrophic or necrotrophic growth in the plant. Active plant defense mechanisms obviously force the selection of microbe variants which can evade the plant's recognition capabilities. This evolutionary tug of war has led to a complex set of both plant and microbe genes, whose interactions lead to a successful plant resistance reaction. As well as a potentially large array of recognition gene functions, a number of subsequent signal transduction steps must be necessary to generate a completely effective resistant phenotype.

Genetic analyses in many systems over the last 50 years have demonstrated that recognition functions are provided by dominant alleles of genes in the plant (Resistance, or R-genes) which interact, either directly or indirectly, with either the direct or indirect product of a single pathogen gene (avirulence, or avr genes). This so called "gene-for-gene" hypothesis is a genetic explanation for interactions between plants and all classes of pathogens: fungal, bacterial, viral, and insect. In the last two years, eight new resistance genes were cloned from various species, and they share certain structural features.

We use a model plant species, Arabidopsis thaliana to identify genetically the plant loci necessary for a resistance reaction against phytopathogenic bacteria and fungus. Our work revolves around four themes. First, isolation of recognition function genes (R or Resistance genes). We use mutation analysis to identify loci which give rise to either loss of recognition, or constitutive induction of a resistance-like phenotype. Second, we isolated mutants in processes involved in control of plant cell death. Third, we are cloning a cluster of R genes directed against a fungal pathogen with the express intent to understand evolution of both R protein function and the evolution of specificity. Fourth, we are identifying the bacterial pathogen genes which are causal to triggering of a specific plant defense response.